Venoso Flashcards
1
Q
- Name some examples of intravenous anesthetics. What are the potential clinical uses of intravenous anesthetics?
A
- Examples of intravenous (IV) anesthetics include the barbiturates, benzodiazepines, opioids, etomidate, propofol, ketamine, and dexmedetomidine. These drugs can be used as induction agents or, in combination with other anesthetics, for the maintenance of anesthesia. Some, particularly propofol and dexmedetomidine, are appropriate for sedation of mechanically ventilated patients in the intensive care unit (ICU). (104)
2
Q
- Explain the concept of “balanced anesthesia.” In addition to intravenous anesthetics, what classes of drugs may be used to provide balanced anesthesia?
A
- “Balanced anesthesia” is the idea of combining various classes of drugs to achieve hypnosis, amnesia, analgesia, and immobility. Inhaled anesthetics, neuromuscular blocking agents, and opioids are often combined with IV anesthetics to achieve balanced anesthesia. (104)
3
Q
- What is similar about the mechanism of action of propofol, barbiturates, benzodiazepines, and etomidate?
A
- Propofol, barbiturates, benzodiazepines, and etomidate all work predominantly by activating or potentiating inhibitory currents through the γ-aminobutyric acid type A (GABAA) chloride channel, leading to a decrease in synaptic transmission in the central nervous system (CNS). However, the exact electrophysiologic effects and GABAA receptor binding sites differ among the drugs. (105)
4
Q
- Describe the chemical structure and physical properties of propofol.
A
- Propofol is a phenol ring derivatized at both ortho-positions (2 and 6) by isopropyl groups (an alkylphenol). It is highly lipid soluble and is formulated as an emulsion with soybean oil, glycerol, and purified egg yolk phosphatide. (105)
5
Q
- Why is it necessary for the manufacturer to include a preservative in propofol emulsions, and why is strict aseptic technique a must during handling?
A
- Propofol emulsions are a rich media that readily support bacterial growth. The manufacturer adds ethylenediaminetetraacetic acid (EDTA) or metabisulfite as a preservative. Vials or syringes of propofol should be discarded within 12 hours after opening, and strict aseptic technique must be followed to prevent fever or sepsis. (105)
6
Q
- Which patients may be at risk for a life-threatening allergic reaction to propofol?
A
- Patients with a history of atopy or allergy to drugs containing a phenyl nucleus or isopropyl group may be at risk. However, patients with IgE-mediated allergy to egg, soy, or peanut are not at increased risk. Patients with sulfite allergy or very reactive airways may require a formulation with EDTA as preservative. (105)
7
Q
- If the elimination half-life of propofol is slow (4 to 24 hours), why do patients awaken rapidly, within 8 to 10 minutes, after a single bolus injection?
A
- Awakening after a single bolus of propofol is determined by rapid redistribution from the brain to less well-perfused tissues (such as skeletal muscle) rather than by elimination. (105)
8
Q
- How is propofol cleared from the plasma?
A
- Propofol is rapidly cleared from the plasma by redistribution to inactive tissue sites and by rapid metabolism in the liver. The lungs may also play a role, accounting for up to 30% of the clearance. (105)
9
Q
- What degree of metabolism does propofol undergo? How should the dose of propofol be altered when administered to patients with liver dysfunction?
A
- Propofol is extensively metabolized by the liver to inactive, water-soluble metabolites that are excreted in the urine. In patients with advanced liver dysfunction, although the volume of distribution increases and protein binding decreases, routine dose adjustment for a single bolus is generally not required. (105)
10
Q
- Define the context-sensitive half-time for a drug. How does the context-sensitive half-time of propofol compare to other intravenous anesthetics?
A
- The context-sensitive half-time is the time needed for the plasma concentration of a drug to decrease by 50% after discontinuation of an infusion, with this time dependent on the duration of the infusion. Propofol has a shorter context-sensitive half-time compared with most barbiturates and benzodiazepines, which explains the rapid recovery after prolonged infusions. (106)
11
Q
- What is the mechanism of action of propofol?
A
- Propofol exerts its effects primarily through the potentiation of the GABAA receptor, prolonging the duration of chloride channel opening and thereby inhibiting neuronal activity. (106)
12
Q
- How does the emergence from a propofol anesthetic or propofol induction differ from the emergence seen with the other induction agents?
A
- Patients emerge rapidly from propofol anesthesia with minimal residual CNS effects, often accompanied by a sense of well-being and mild euphoria, which distinguishes it from other induction agents. (106)
13
Q
- How does propofol affect the central nervous system?
A
- Propofol decreases the cerebral metabolic rate for oxygen (CMRO2), cerebral blood flow (CBF), and intracranial pressure (ICP) in a dose-dependent manner, and at high doses it produces burst suppression on the EEG. (106)
14
Q
- How does propofol affect the seizure threshold?
A
- Propofol has anticonvulsant properties and is used to treat seizures, though transient excitatory muscle twitching may occur without indicating true seizure activity. (106)
15
Q
- How does propofol affect the cardiovascular system?
A
- Propofol causes a significant decrease in systolic blood pressure, primarily due to venous and arterial vasodilation, reduced preload, and decreased systemic vascular resistance (SVR), with little compensatory increase in heart rate. (107)
16
Q
- How does propofol affect ventilation?
A
- Propofol produces a dose-dependent depression of ventilation, often resulting in transient apnea following an induction dose, with a decrease in both respiratory rate and tidal volume during maintenance. (107)
17
Q
- How does propofol affect the upper airway and airway reflexes?
A
- Propofol markedly reduces upper airway reflexes, facilitating airway instrumentation; however, it also increases the collapsibility of the upper airway, which may predispose to obstruction during emergence or sedation. (107)
18
Q
- What is the propofol infusion syndrome, and what clinical findings should prompt investigation for it?
A
- Propofol infusion syndrome is a rare but potentially fatal condition associated with high-dose propofol infusions (>4 mg/kg/h) characterized by metabolic acidosis, rhabdomyolysis, hyperkalemia, fever, arrhythmias, ECG changes, hypertriglyceridemia, hepatomegaly, renal failure, or heart failure. (107)
19
Q
- How can the pain associated with the intravenous injection of propofol be attenuated?
A
- Injection pain can be minimized by using large antecubital veins, prior administration of lidocaine, premedication with an opioid, or by mixing lidocaine with propofol. (107)
20
Q
- What is a typical induction dose of propofol? Describe at least two patient populations in which this dose should be adjusted.
A
- Typical induction doses range from 1 to 2.5 mg/kg IV. Dose adjustments are recommended in the elderly (lower dose due to decreased requirements and reduced volume of distribution) and in morbidly obese patients (dose based on lean body weight). (107)
21
Q
- How is propofol administered for maintenance anesthesia?
A
- Propofol is administered for maintenance anesthesia via continuous IV infusion at rates of 100 to 200 µg/kg/min, titrated to clinical signs of anesthesia. (107)
22
Q
- What is total intravenous anesthesia (TIVA)?
A
- TIVA is a technique where general anesthesia is maintained solely by IV anesthetics, most commonly propofol, often combined with other sedative-hypnotics, opioids, or analgesics, without the use of volatile agents. (107)
23
Q
- How is propofol administered for sedation?
A
- Propofol is used for sedation via continuous IV infusion at lower rates (25 to 75 µg/kg/min), providing sedation and likely amnesia without complete hypnosis. (107)
24
Q
- What is the relationship between propofol and nausea and vomiting?
A
- Propofol has a significant antiemetic effect, resulting in a lower incidence of postoperative nausea and vomiting (PONV), and can also be used to treat nausea in subhypnotic doses. (107-108)
25
Q
- How are the structure and physicochemical properties of fospropofol different from propofol?
A
- Fospropofol is a water-soluble phosphate ester prodrug of propofol, metabolized by alkaline phosphatase to produce propofol, phosphate, and formaldehyde; this formulation eliminates the need for a lipid emulsion. (108)
26
Q
- What are the advantages and disadvantages of fospropofol compared with propofol?
A
- Advantages of fospropofol include reduced risk of bacterial contamination and less injection pain. Disadvantages include a slower onset, prolonged recovery, and frequent perineal burning or pruritus. (108)
27
Q
- What are the clinical uses of fospropofol?
A
- In the United States, fospropofol is approved for sedation during monitored anesthesia care, particularly for procedures such as endoscopy, bronchoscopy, and minor surgical interventions. (108)
28
Q
- Name some of the barbiturates. From what chemical compound are they derived?
A
- Common barbiturates include thiopental and methohexital, among others like pentobarbital, phenobarbital, and thiamylal. They are derivatives of barbituric acid. (108)
29
Q
- What other drug formulations and fluids are incompatible to inject with barbiturates?
A
- Barbiturates, formulated as sodium salts in alkaline solutions, are incompatible with acidic preparations such as neuromuscular blockers, ketamine, midazolam, certain opioids (alfentanil, sufentanil), some catecholamines, and lactated Ringer’s solution. (109)
30
Q
- How are barbiturates cleared from the plasma?
A
- Barbiturates are primarily cleared from the plasma through rapid redistribution to inactive tissue sites after bolus administration. (109)
31
Q
- Describe the metabolism of barbiturates and their interactions with the microsomal P450 system.
A
- Barbiturates are extensively metabolized in the liver via oxidation, N-dealkylation, desulfuration, and ring breakdown; they are excreted as polar metabolites in urine or bile. Barbiturates can induce microsomal P450 enzymes, and their metabolism is increased by enzyme inducers. (109)
32
Q
- What is the effect-site equilibration time of barbiturates relative to other intravenous anesthetics?
A
- The effect-site equilibration time for barbiturates is short (approximately 30 seconds after rapid IV injection) due to rapid brain uptake, comparable to propofol; methohexital equilibrates slightly faster than thiopental. (110-111)
33
Q
- What is the context-sensitive half-time of barbiturates relative to other intravenous anesthetics?
A
- The context-sensitive half-time of barbiturates increases with prolonged infusion and is longer than that of propofol for comparable durations. (110-111)
34
Q
- How do methohexital and thiopental compare with regard to induction doses, duration of action, and clinical utility?
A
- Methohexital is used at an induction dose of 1 to 1.5 mg/kg and has a shorter duration of action with rapid awakening, making it suitable for outpatient procedures (e.g., ECT), whereas thiopental is used at 3 to 5 mg/kg and has a longer duration. (110-111)
35
Q
- What is the mechanism of action of barbiturates?
A
- Barbiturates act by potentiating the effects of GABA at the GABAA receptor, increasing the duration of chloride channel opening and hyperpolarizing neurons, thus inhibiting synaptic transmission. (110-111)
36
Q
- How do barbiturates affect the central nervous system? How do barbiturates affect an electroencephalogram?
A
- Barbiturates depress CNS activity; thiopental produces a dose-dependent depression of the EEG (potentially leading to burst suppression), while methohexital may paradoxically stimulate epileptic foci. (110-111)
37
Q
- How do barbiturates affect the arterial blood pressure?
A
- Barbiturates typically cause a modest decrease in arterial blood pressure, primarily due to peripheral vasodilation and reduced preload. (110-111)
38
Q
- How do barbiturates affect the heart rate?
A
- Barbiturates usually cause an increase in heart rate via a baroreceptor reflex in response to hypotension, although overall cardiac output may still decrease. (110-111)
39
Q
- How do barbiturates affect ventilation?
A
- Barbiturates depress ventilation by reducing the responsiveness of the medullary ventilatory centers, often leading to slow, shallow breathing and possible transient apnea. (110-111)
40
Q
- How do barbiturates affect laryngeal and cough reflexes?
A
- Induction doses of thiopental alone do not reliably suppress laryngeal and cough reflexes; additional measures (e.g., neuromuscular blockers or adjuncts) may be required to prevent airway stimulation. (110-111)
41
Q
- What are some potential adverse complications of the injection of thiopental?
A
- Adverse complications include intense pain and vasoconstriction following accidental intra-arterial injection (which may lead to gangrene), tissue irritation and necrosis with subcutaneous injection, and venous thrombosis due to barbiturate crystallization. (110-111)
42
Q
- What is the risk of a life-threatening allergic reaction to barbiturates?
A
- Life-threatening allergic reactions to barbiturates are rare, with an estimated risk of 1 in 30,000. (111)
43
Q
- What are the various routes and methods for the administration of barbiturates in clinical anesthesia practice?
A
- Barbiturates can be administered rapidly IV for induction, given in small IV boluses for mask acceptance, or via rectal administration (e.g., methohexital in young or uncooperative patients). (111)
44
Q
- How should thiopental be administered and dosed for cerebral protection in patients with persistently elevated intracranial pressures?
A
- High doses of thiopental can be titrated (often guided by EEG showing burst suppression) to reduce ICP, ensuring that MAP and CPP are maintained; its use is considered in patients with intracranial space-occupying lesions. (111)
45
Q
- What is barbiturate coma? What are some potential complications?
A
- Barbiturate coma refers to the deliberate, high-dose infusion of a barbiturate (usually thiopental) to achieve complete EEG suppression for neuroprotection. Potential complications include hemodynamic instability, electrolyte imbalances, arrhythmias, immunosuppression, and the need for invasive monitoring. (111)
46
Q
- Name some of the commonly used benzodiazepines. What are some of the clinical effects and properties of benzodiazepines that make them useful in anesthesia practice?
A
- Common benzodiazepines include midazolam, diazepam, and lorazepam. They provide anxiolysis, sedation, and anterograde amnesia, with minimal cardiopulmonary depression and anticonvulsant effects, making them useful for premedication, induction, sedation, and seizure suppression. (112)
47
Q
- How does water-soluble midazolam cross the blood-brain barrier to gain access to the central nervous system?
A
- Midazolam is initially hydrophilic and exists in an open-ring form at low pH; when exposed to the higher pH of blood, it undergoes ring closure, becomes highly lipid soluble, and rapidly crosses the blood-brain barrier. (112)
48
Q
- How are benzodiazepines metabolized? How does the metabolism of lorazepam differ from that of other benzodiazepines?
A
- Most benzodiazepines undergo oxidative metabolism by microsomal P450 enzymes followed by glucuronidation. Lorazepam, temazepam, and oxazepam do not undergo oxidation but are directly conjugated, making lorazepam less susceptible to drug interactions. (112)
49
Q
- How do the metabolites of diazepam and midazolam differ?
A
- Diazepam is metabolized to long-acting active compounds (desmethyldiazepam and oxazepam), while midazolam produces a single active metabolite (1-hydroxymidazolam) that is rapidly cleared in healthy individuals but may accumulate in liver or renal dysfunction. (112)
50
Q
- What is the effect-site equilibration time of benzodiazepines relative to other intravenous anesthetics?
A
- Benzodiazepines have a short effect-site equilibration time, though it is slower than propofol or thiopental; their duration of action after a bolus is dependent on redistribution. (112)
51
Q
- How do the context-sensitive half-times of the benzodiazepines compare to each other and to other classes of intravenous anesthetics?
A
- The context-sensitive half-time of benzodiazepines, particularly diazepam and lorazepam, is prolonged compared with midazolam and is generally longer than that of propofol for similar infusion durations. (112)
52
Q
- What is remimazolam? Name two other commonly used drugs that are metabolized by a similar mechanism.
A
- Remimazolam (CNS 7056) is an ultra-short-acting benzodiazepine that is rapidly hydrolyzed by blood and tissue esterases. Remifentanil and esmolol are examples of drugs also metabolized via ester hydrolysis. (112)
53
Q
- What is the mechanism of action of benzodiazepines?
A
- Benzodiazepines bind to the GABAA receptor and enhance the inhibitory effects of GABA by increasing the duration of chloride channel opening, resulting in neuronal hyperpolarization. (112-113)
54
Q
- Where are benzodiazepine receptors located?
A
- Benzodiazepine receptors (associated with the GABAA ion channel) are primarily located on postsynaptic nerve endings in the CNS, with the greatest density in the cerebral cortex. (113)
55
Q
- Describe the overall macromolecular structure of the γ-aminobutyric acid type A (GABAA) receptor. Is the structure typically constant or subject to variation?
A
- The GABAA receptor is a pentameric ion channel typically composed of two α, two β, and one γ subunit; there is significant subunit diversity which contributes to variable receptor function in the CNS. (113)
56
Q
- How do midazolam, diazepam, and lorazepam compare with regard to affinity for the benzodiazepine receptor?
A
- Lorazepam has the highest affinity, followed by midazolam, and then diazepam. (113)
57
Q
- How do benzodiazepines affect the central nervous system?
A
- Benzodiazepines decrease cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) in a dose-dependent manner, enhance inhibitory neurotransmission, raise the seizure threshold, and produce sedation and anterograde amnesia without inducing an isoelectric EEG. (113)
58
Q
- How do benzodiazepines affect the cardiovascular system?
A
- Benzodiazepines generally produce minimal cardiovascular depression, though induction doses (especially of midazolam) may decrease blood pressure due to decreased systemic vascular resistance. (113)
59
Q
- How do benzodiazepines affect ventilation and the upper airway?
A
- Benzodiazepines have dose-dependent ventilatory depressant effects and may impair pharyngeal coordination, increasing the risk of upper airway obstruction and pulmonary aspiration. (113)
60
Q
- Which organic solvent is used to dissolve diazepam into solution? What are some of the effects of this solvent?
A
- Propylene glycol is used to dissolve diazepam; it can lead to unpredictable absorption when given intramuscularly and is responsible for pain and potential thrombophlebitis when diazepam is administered IV. (113)
61
Q
- How common are allergic reactions to benzodiazepines?
A
- Allergic reactions to benzodiazepines are extremely rare. (113)
62
Q
- What are some clinical uses of benzodiazepines in anesthesia practice?
A
- Benzodiazepines are used for preoperative medication, IV sedation, induction of anesthesia, and suppression of seizure activity. (114)
63
Q
- How do midazolam, diazepam, and lorazepam compare with regard to time of onset and degree of amnesia when administered for sedation?
A
- Midazolam has a rapid onset and produces more pronounced amnesia compared to diazepam and lorazepam; when given orally, peak plasma concentrations occur in about 30 minutes for midazolam, 60 minutes for diazepam, and 2 hours for lorazepam. (114)
64
Q
- What are some considerations the anesthesiologist should be aware of when deciding whether or not to use midazolam as premedication before elective or outpatient procedures?
A
- Considerations include the potential for prolonged sedation and anterograde amnesia, which may interfere with the patient’s ability to recall preoperative instructions; therefore, important information should be provided in writing or to a family member. (114-115)
65
Q
- Describe some features of the amnesia induced by midazolam and its importance to anesthesiologists and surgeons when counseling patients and families.
A
- Midazolam produces anterograde amnesia without affecting memories formed prior to its administration; however, patients may not recall events in the preoperative area, so critical information should be communicated clearly and in an alternative format. (115)
66
Q
- Describe dosage and strategies for induction of general anesthesia with midazolam. Why is midazolam preferred over other benzodiazepines for this purpose? What are some advantages and disadvantages of benzodiazepines for use as induction agents?
A
- The IV induction dose of midazolam is 0.1 to 0.3 mg/kg with an onset of 30 to 80 seconds. It is preferred due to its relatively rapid onset and reliability in producing amnesia, though disadvantages include delayed awakening and lack of analgesia. (115)
67
Q
- How can the effects of benzodiazepines be reversed?
A
- The effects of benzodiazepines can be reversed with flumazenil, a competitive antagonist that is titrated in 0.2 mg IV increments every 60 seconds (up to 1–3 mg total), though its duration of action is about 20 minutes. (115)
68
Q
- What is the optimal choice, dose, and route of benzodiazepine for treatment of status epilepticus in hospitalized patients? How does it differ in prehospital treatment of status epilepticus?
A
- For in-hospital status epilepticus, IV lorazepam at 0.1 mg/kg is preferred; if IV access is unavailable in the prehospital setting, 5–10 mg of intramuscular midazolam is recommended. (115)
69
Q
- What chemical compound is ketamine a derivative of?
A
- Ketamine is a derivative of phencyclidine (PCP). (115)
70
Q
- How does the anesthetic state induced by ketamine differ from other intravenous anesthetics?
A
- Ketamine produces a dissociative anesthesia characterized by unresponsiveness, amnesia, and profound analgesia, which is distinct from the sedation and hypnosis produced by other IV agents. (115)
71
Q
- How do patients appear clinically after an induction dose of ketamine?
A
- After an induction dose of ketamine, patients typically appear cataleptic with eyes open, a slow nystagmic gaze, maintained cough, swallow, and corneal reflexes, moderate pupil dilation, lacrimation, salivation, and increased skeletal muscle tone with purposeless movements. (115)
72
Q
- What is the mechanism by which the effects of ketamine are terminated?
A
- Ketamine is rapidly redistributed from the brain to inactive tissues and is extensively metabolized in the liver to norketamine, which has about 20–30% of the potency of ketamine, facilitating rapid recovery after a bolus. (115)
73
Q
- What is the mechanism of action of ketamine?
A
- Ketamine primarily exerts its effects by inhibiting the N-methyl-D-aspartate (NMDA) receptor complex, while also interacting with µ-opioid receptors, monoaminergic receptors, muscarinic receptors, and calcium channels. (115-116)
74
Q
- How does ketamine affect the central nervous system?
A
- Ketamine causes CNS excitation, increases cerebral blood flow, intracranial pressure, and cerebral metabolism, and produces beta and gamma wave activity on the EEG. (116)
75
Q
- How does ketamine affect the cardiovascular system?
A
- Ketamine increases systemic blood pressure, pulmonary artery pressure, heart rate, and cardiac output via sympathetic stimulation, though these effects may be blunted in catecholamine-depleted states. (116)
76
Q
- How does ketamine affect ventilation?
A
- Ketamine may cause transient depression of ventilation or apnea with large doses but typically preserves or even increases airway patency due to bronchodilation; it also increases airway secretions. (116)
77
Q
- How does ketamine affect skeletal muscle tone? How does this affect the upper airway?
A
- Ketamine preserves or may increase skeletal muscle tone, which helps maintain a patent upper airway and preserves protective reflexes, although it does not guarantee airway protection against regurgitation. (116)
78
Q
- What are the induction doses for ketamine given by the intravenous and intramuscular routes? What is the time of onset for each route?
A
- The IV induction dose is 1–2 mg/kg (onset within 60 seconds) and the IM dose is 5–10 mg/kg (onset within 2–4 minutes); full recovery from an IV dose usually takes 10–20 minutes, with full orientation in 60–90 minutes. (116)
79
Q
- What does the emergence delirium associated with ketamine refer to? What is the incidence? How can it be prevented?
A
- Emergence delirium refers to a state of vivid dreaming, illusions, and a sense of detachment during recovery, with an incidence of up to 30%; it may be reduced by administering benzodiazepines pre- or post-induction. (116)
80
Q
- What are some common clinical uses of ketamine?
A
- Ketamine is used for induction in hypovolemic patients, IM induction in uncooperative children or developmentally disabled patients, procedural sedation, and for analgesia during dressing changes in burn patients. (116)
81
Q
- What can the repeated administration of ketamine lead to? How does it manifest clinically?
A
- Repeated ketamine administration may lead to tolerance to its analgesic effects, necessitating higher doses to achieve the same effect, as seen in patients undergoing multiple procedures such as burn dressing changes. (116)
82
Q
- How common are allergic reactions to ketamine?
A
- Allergic reactions to ketamine are uncommon. (116)
83
Q
- Name a common psychiatric condition that ketamine may be used to treat.
A
- Ketamine has shown promise in the treatment of treatment-resistant major depression. (117)
84
Q
- What type of structure is etomidate? Name another intravenous anesthetic that shares this structure.
A
- Etomidate is an imidazole derivative; dexmedetomidine and midazolam also contain imidazole groups. (117)
85
Q
- How is etomidate cleared from the plasma?
A
- Etomidate is rapidly cleared from the plasma via nearly complete ester hydrolysis by the liver, with less than 3% excreted unchanged in the urine. (117)
86
Q
- What degree of metabolism does etomidate undergo?
A
- Etomidate undergoes nearly complete ester hydrolysis, resulting in inactive metabolites. (117)
87
Q
- What is the context-sensitive half-time of etomidate relative to other intravenous anesthetics? What is the effect-site equilibration time of etomidate relative to other intravenous anesthetics?
A
- Etomidate has one of the shortest context-sensitive half-times among IV anesthetics, similar to thiopental and propofol, due to rapid redistribution and a short effect-site equilibration time. (117)
88
Q
- What is the mechanism of action of etomidate?
A
- Etomidate acts predominantly as a GABAA receptor agonist, similar to propofol, benzodiazepines, and barbiturates, although its specific binding site likely differs from the others. (117)
89
Q
- How does etomidate affect the central nervous system?
A
- Etomidate is a cerebral vasoconstrictor that decreases cerebral blood flow, intracranial pressure, and cerebral metabolic rate for oxygen, and can be titrated to achieve burst suppression on the EEG. (117)
90
Q
- How does etomidate affect the seizure threshold?
A
- Etomidate increases the activity of seizure foci on the EEG and may cause myoclonus in over half of patients, similar to methohexital. (117)
91
Q
- How does etomidate affect the cardiovascular system?
A
- Etomidate produces minimal changes in heart rate, MAP, central venous pressure, stroke volume, or cardiac index, making it useful for induction in patients with limited cardiac reserve, although some hypotension may occur in hypovolemic patients. (117)
92
Q
- How does etomidate affect ventilation?
A
- Etomidate causes less respiratory depression than propofol or thiopental when administered alone, though respiratory depression may occur when combined with other anesthetics or opioids. (117)
93
Q
- What are the endocrine effects of etomidate?
A
- Etomidate inhibits 11β-hydroxylase, leading to suppression of cortisol synthesis and adrenocortical function for at least 4 to 8 hours (and possibly up to 48 hours) after an induction dose. (117)
94
Q
- Name specific patient populations that may benefit from choice of etomidate as an induction agent.
A
- Patients with limited cardiac reserve, such as those with coronary artery disease, critical aortic stenosis, or hypovolemia, as well as patients with head trauma or elevated ICP, may benefit from etomidate induction. (117)
95
Q
- What are some potential negative effects associated with the administration of etomidate?
A
- Negative effects of etomidate include injection pain, superficial thrombophlebitis, myoclonus, increased incidence of postoperative nausea and vomiting (PONV), and adrenocortical suppression. (118)
96
Q
- What type of structure is dexmedetomidine? How is it cleared from the plasma?
A
- Dexmedetomidine is the active S-enantiomer of medetomidine, an imidazole derivative. It is rapidly metabolized in the liver, with metabolites excreted via bile and urine; its context-sensitive half-time increases with longer infusions. (118)
97
Q
- What is the mechanism of action for dexmedetomidine?
A
- Dexmedetomidine is a highly selective α2-adrenergic agonist that produces sedation, analgesia, and sympatholysis by activating α2 receptors in the CNS (including the locus ceruleus) and spinal cord. (118)
98
Q
- How does the sedation produced by dexmedetomidine differ from that of other intravenous anesthetics?
A
- Dexmedetomidine produces sedation that resembles natural sleep, with patients who are easily arousable and cooperative, unlike the deep sedation produced by agents such as propofol. (119)
99
Q
- What are the effects of dexmedetomidine on cerebral blood flow?
A
- Dexmedetomidine likely decreases cerebral blood flow without significantly changing intracranial pressure or cerebral metabolic rate for oxygen. (119)
100
Q
- How does dexmedetomidine affect the electroencephalogram?
A
- The EEG of patients receiving dexmedetomidine shows features similar to physiologic sleep, such as spindles, without the burst suppression seen with deeper anesthesia. (119)
101
Q
- How does dexmedetomidine infusion affect the cardiovascular system?
A
- Dexmedetomidine infusions decrease heart rate and blood pressure by reducing sympathetic outflow, although bolus injections can transiently increase blood pressure due to peripheral vasoconstriction. (119)
102
Q
- Compare the hemodynamic effects of a bolus injection or rapid loading dose of dexmedetomidine with the hemodynamic effects of an infusion.
A
- A rapid bolus or loading dose of dexmedetomidine may cause transient hypertension and marked bradycardia, whereas a slow infusion produces more gradual decreases in heart rate and blood pressure. (119)
103
Q
- How does dexmedetomidine affect the respiratory system?
A
- Dexmedetomidine has minimal respiratory depressant effects compared with other IV anesthetics, causing only small decreases in tidal volume with little change in respiratory rate. (119)
104
Q
- What are the typical doses for dexmedetomidine when used as an infusion in the operating room?
A
- Typical dosing for dexmedetomidine during general anesthesia is a loading dose of 0.5–1 µg/kg over 10–15 minutes followed by an infusion of 0.2–0.7 µg/kg/h. (119)
105
Q
- What are some common clinical uses for dexmedetomidine?
A
- Dexmedetomidine is used as an adjunct during general anesthesia, for procedural sedation, for awake fiberoptic intubation, and for sedation of mechanically ventilated patients in the ICU. (119)
